It has been known for many years that pressure in the region of the carotid sinus might produce slowing of the heart, unconsciousness, and convulsions. These effects were ascribed to stimulation of the vagus nerve until the anatomic and physiological studies of Hering.1 Weiss and Baker2in 1933 called attention to the fact that a hypersensitive carotid sinus reflex was responsible for spontaneous attacks of vertigo, syncope, convulsions, and lesser symptoms. They described three types of carotid sinus syndrome: (1) the cardioinhibitory, or vagal, type with cardiac slowing or asystole, which is prevented by atropine; (2) the vasodepressor type, in which there is a decided drop in blood pressure not related to bradycardia, which may be prevented by epinephrine but not atropine; and (3) the cerebral type, in which there is loss of consciousness without significant cardiac slowing or drop in blood pressure and is not affected by